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p53 post-translational modification: deregulated in tumorigenesis

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TRENDS IN MOLECULAR MEDICINE
卷 16, 期 11, 页码 528-536

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ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2010.09.002

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  1. NCI NIH HHS [R01 CA129627, R01 CA131439, R01 CA118561, P01 CA080058, R01 CA085533, P01 CA097403] Funding Source: Medline

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The p53 tumor suppressor protein has well-established roles in monitoring various types of stress signals by activating specific transcriptional targets that control cell cycle arrest and apoptosis, although some activities are also mediated in a transcription-independent manner. Here, we review the recent advances in our understanding of the wide spectrum of post-translational modifications that act as epigenetic-like codes for modulating specific functions of p53 in vivo and how deregulation of these modifications might contribute to tumorigenesis. We also discuss future research priorities to further understand p53 post-translational modifications and the interpretation of genetic data in appreciation of the increasing evidence that p53 regulates cellular metabolism, autophagy and many unconventional tumor suppressor activities.

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